Because we have previously found that a subcutaneus injection of basic fibroblast growth factor over 12 hours in the rat could cause endothelial cell DNA synthesis, we sought to learn something about the pharmacokinetics of these injections. Because of the limited availability of these growth factors and previous observations that heparin could enhance the binding of the acidic form of fibroblast growth factor, also known as endothelial cell growth factor, we selected this growth factor and injected it with and without heparin into rats intravenously, after pretreatment with sodium iodide to prevent binding of the radioactive iodine moiety which we used to label the endothelial cell growth factor. We found that the radiolabeled growth factor bound to all organs and in particular to the kidney, followed by the liver, on a dry weight basis. The least binding was to the brain. Because the kidney and liver have porous capillaries and filter the plasma through a large amount of subendothelial tissue rich in glycosaminoglycans, we suggest that the endothelial cell growth factor might bind to these components of the extracellular matrix. The low amount of binding the brain could relate to the very tight junctions between endothelial cells which constitute the blood-brain barrier. We also found that heparin enhanced the binding of ECGF to all organs, as it does to cultured cells. The exception was the kidney, which bound less ECGF when it was injected with an excess of heparin, perhaps indicating that the ECGF heparin binding sites were already occupied. The 4 fold increase in the circulating half life of the growth factor (to 60 seconds) and the enhanced endothelial binding (to organs other than kidney) suggest that heparin may enhance the utility of ECGF as an investigative therapy to promote angiogenesis and wound healing.